Citrus canker, induced by bacterial infection, seriously affects the growth and productivity of citrus around the world and has attracted strong research interest. The current treatment for this disease uses copper salts to inactivate the pathogenic bacteria: Xanthomonas citri subsp. citri ( Xcc ) strain. However, copper salts may have a negative impact on the environment or plant. In this work, we identify a chemical compound, 2,6-diiodo-1,3,5,7-tetramethyl-8-(P-benzoic acid)-4,4′-difluoroboradiazaindacene (DIBDP), to inactivate the pathogenic Xcc strain ( 29-1 ). DIBDP is activated by sunlight and generates reactive oxygen species to kill the bacteria. In order to overcome the degradation of DIBDP under sunlight, an adjuvant agent was identified to limit the photodegradation of DIBDP by forming a photosensitizer complex (PSC). This complex demonstrated significant antimicrobial activity to Xcc 29-1 , which was 64-fold more potent than the copper biocides. The antimicrobial efficacy of PSC on citrus leaves infected by Xcc 29-1 also was much stronger than copper agent and, at the same time, the PSC was safe to the host exposed to sunlight. Thus, this PSC is a promising antibacterial agent to control citrus canker disease.
The invasion and colonization of host plants by the destructive pathogen Ralstonia solanacearum relies on its cell motility, which is controlled by multiple factors. Here, we report that the LysR-type transcriptional regulator CrgA (RS_RS16695) represses cell motility in R. solanacearum GMI1000. CrgA possesses common features of a LysR-type transcriptional regulator and contains an N-terminal helix-turn-helix motif as well as a C-terminal LysR substrate-binding domain. Deletion of crgA results in an enhanced swim ring and increased transcription of flhDC. In addition, ΔcrgA possesses more polar flagella than wild-type GMI1000 and exhibits higher expression of the flagellin gene fliC. Despite these alterations, ΔcrgA did not have a detectable growth defect in culture. Yeast one-hybrid and electrophoretic mobility shift assays revealed that CrgA interacts directly with the flhDC promoter. Expressing the GUS reporter under the control of the crgA promoter showed that crgA transcription is dependent on cell density. Soil-soaking inoculation with the crgA mutant caused wilt symptoms on tomato (Solanum lycopersicum L. cv. Hong yangli) plants earlier than inoculation with the wild-type GMI1000 but resulted in lower disease severity. We conclude that the R. solanacearum regulator CrgA represses flhDC expression and consequently affects the expression of fliC to modulate cell motility, thereby conditioning disease development in host plants. Importance Ralstonia solanacearum is a widely distributed soil-borne plant pathogen that causes bacterial wilt disease on diverse plant species. Motility is a critical virulence attribute of R. solanacearum because it allows this pathogen to efficiently invade and colonize host plants. In R. solanacearum, motility defective strains are markedly affected in pathogenicity, which is coregulated with multiple virulence factors. In this study, we identified a new LysR-type transcriptional regulator (LTTR), CrgA, that negatively regulates motility. The mutation of the corresponding gene leads to precocious appearance of wilt symptoms on tomato plants when the pathogen is introduced using soil-soaking inoculation. This study indicates that the regulation of R. solanacearum motility is more complex than previously thought and enhances our understanding of flagellum regulation in R. solanacearum.
Background: 'Candidatus Liberibacter asiaticus' (Las) is the pathogenic bacterium that causes Huanglongbing in citrus plants, as well as in several types of experimental plants. Las releases a set of effectors to modulate host responses. One of these critical effectors is Sec-delivered effector 1 (SDE1), which induces chlorosis in Nicotiana benthamiana. Results: Four SDE1-interacting proteins were identified from N. benthamiana, including DEAD-box RNA helicase DDX3, 26S proteasome non-ATPase regulatory subunit PSMD14, an ARM repeat protein, and a hypothetical protein. Gene silencing revealed that knockdown of the NbDDX3 gene led to chlorosis in N. benthamiana leaves. Fluorescent signal detection revealed that SDE1 was localized to the cell membrane, cytoplasm, and nucleus. Simultaneously, NbDD3 was expressed in cytoplasmic vesicles, as well as in the cell membrane. The interactions between SDE1 and NbDDX3 were shown to be localized on cell membrane using co-localization and bimolecular fluorescence complementation analysis. Moreover, the transcription of NbDDX3 gene was substantially suppressed in N. benthamiana plants that expressed SDE1. Conclusion: Las effector SDE1 interacts with NbDDX3 at the cell membrane. Most importantly, the transient expression of SDE1 exerts a suppression effect on the transcription of NbDDX3 gene. The silencing of NbDDX3 leads to leaf chlorosis in N. benthamiana. This provided evidence to understand the molecular events in association with chlorosis induced by SDE1.
A recyclable peroxidase mimic Fe3O4@polydopamine/prussian blue (Fe3O4@PDA/PB) composite was facilely prepared by coating of PDA on Fe3O4 nanoparticle core and in situ growth of PB nanoparticles on PDA shell. The...
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